Electrocardiographic manifestations of hyperkalemia

Mattu, Amal; Brady, William J.; Robinson, David

doi:10.1053/ajem.2000.7344

Cited by 200 publications

(122 citation statements)

References 18 publications

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“…The changes of ECG parameters including widened QRS complex, decreased P wave amplitude and bradycardia found in this study (Figs 3 and 4) are common findings in HK, which is entirely consistent with early reports (Kuvin, 1998;Mattu et al, 2000;Mehta et al, 2001). O'Neill and Paterson (1995) demonstrated in the anaesthetised pig that cardiac sympathetic nerve stimulation or NE infusion both corrected the cardiovascular parameters disturbed by HK.…”

Section: Effects Of Ne and Sal On Ecg Parameterssupporting

confidence: 93%

“…Serum K + levels above 5.5 mmol/L have traditionally been regarded as HK (Chevet, 1998;Mattu et al, 2000;Hummel and Chauveau, 2001). In the present study, infusion of 300 mM KCl solution for 15 min resulted in a more than 7 mmol/l increase in serum K + level (Fig.…”

Section: Induction Of Hkmentioning

confidence: 99%

“…Hyperkalaemia (HK) (serum K + level higher than 5.5 mmol/L) develops when K + regulation is disturbed and may have serious cardiotoxic effects with typical changes of electrocardiography (ECG) findings including decreased heart rate, flattened P wave, prolonged QRS complex, and peaked T wave (Chevet, 1998;Kuvin, 1998;Mattu et al, 2000).…”

mentioning

confidence: 99%

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Experimental hyperkalaemia in rabbits: Effects of salbutamol and norepinephrine treatments on blood biochemistry and electrocardiography

Çeli̇k

Bal

Durgut

2003

Acta Veterinaria Hungarica

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The effects of salbutamol and norepinephrine on the electrocardiogram (ECG), serum potassium level and enzyme activities were studied in rabbits with hyperkalaemia; norepinephrine and salbutamol may be therapeutically useful. For induction of hyperkalaemia, 300 mM KCl solution was used and then isotonic saline solution containing 6 µg salbutamol and 3.9 µg norepinephrine per ml were administered. Norepinephrine and salbutamol decreased the serum potassium from 7.36 ± 0.26 and 7.21 ± 0.31 mmol/L to 5.62 ± 0.27 and 4.35 ± 0.33 mmol/L, respectively, and caused the ECG changes (flatness of P wave, widening of QRS complex and bradycardia) to return to the control conditions (time 0). Norepinephrine, but not salbutamol, decreased the activities of aspartate aminotransferase (AST), alanine aminotransferase (ALT) and lactate dehydrogenase (LDH) to the control levels. These results suggest that monitoring of the enzyme activities might be useful as it yields indexes suitable for evaluating the therapeutic approach with norepinephrine in hyperkalaemia.

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Section: Effects Of Ne and Sal On Ecg Parameterssupporting

confidence: 93%

Section: Induction Of Hkmentioning

confidence: 99%

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Experimental hyperkalaemia in rabbits: Effects of salbutamol and norepinephrine treatments on blood biochemistry and electrocardiography

Çeli̇k

Bal

Durgut

2003

Acta Veterinaria Hungarica

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“…If hyperkalemia is left untreated, a sine-wave pattern, idioventricular rhythms, and asystolic cardiac arrest may develop. 203,204 …”

Section: Hyperkalemiamentioning

confidence: 99%

Part 12: Cardiac Arrest in Special Situations

Hoek¹,

Morrison²,

Shüster³

et al. 2010

Circulation

637

431

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“…This rhythm corresponds to monophasic waves formed by the fusion of the wide QRS complex with the T wave, which simulate a ventricular flutter. 40 Moderate or severe elevations of potassium concentration can lead to an increase of the ST segment in left precordial derivations. These derivations can simulate an ischemic pattern, and can even produce a type I Brugada pattern when it accompanies a complete left branch block.…”

mentioning

confidence: 99%

Hyperkalemia in heart failure patients: current challenges and future prospects

López‐Vilella¹,

Morillas-Climent²,

Plaza-López³

et al. 2016

RRCC

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Abstract:In heart failure (HF), hyperkalemia is a frequent problem because of several factors, such as neurohormonal mechanisms involved in the disease, renal failure, comorbidities, and drugs with a prognostic benefit. These drugs can block the renin-angiotensin-aldosterone system, and therefore, serum potassium levels can increase, mostly when combined with other drugs as nonsteroidal anti-inflammatories, digitalis, heparin, etc. Hyperkalemia can have severe consequences if not corrected, mostly at the cardiac level (decrease in speed conduction, QRS enlargement, ventricular arrhythmias, and asystole). Therefore, it is important to adequately prescribe these potentially harmful drugs (starting at low doses with close monitoring of renal function and potassium levels), to carefully manage the factors that can interfere with potassium levels, and to early treat hyperkalemia if it develops. There are several investigation lines for the design of new molecules that show a similar efficacy to that of renin-angiotensin-aldosterone system, with a lower risk of hyperkalemia: nonsteroidal mineralocorticoid receptor antagonists like finerenone, which is a more cardioselective drug than traditional mineralocorticoid receptor antagonists, and angiotensin and neprilysin inhibitors such as LCZ696, which have proven to reduce mortality and heart failure hospitalizations. Besides, new drugs are being studied, which are able to reduce levels of serum potassium in a sustained and faster way, like chelating polymers Patiromer and sodium zirconium cyclosilicate.

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Electrocardiographic manifestations of hyperkalemia

Cited by 200 publications

References 18 publications

Experimental hyperkalaemia in rabbits: Effects of salbutamol and norepinephrine treatments on blood biochemistry and electrocardiography

Experimental hyperkalaemia in rabbits: Effects of salbutamol and norepinephrine treatments on blood biochemistry and electrocardiography

Part 12: Cardiac Arrest in Special Situations

Hyperkalemia in heart failure patients: current challenges and future prospects

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